Pérez-Cobas Ana E, Artacho Alejandro, Ott Stephan J, Moya Andrés, Gosalbes María J, Latorre Amparo
Unidad Mixta de Investigación en Genómica y Salud de la Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana (FISABIO) y el Instituto Cavanilles de Biodiversidad y Biología Evolutiva de la Universitat de València València, Spain ; CIBER en Epidemiología y Salud Pública Madrid, Spain.
Unidad Mixta de Investigación en Genómica y Salud de la Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunidad Valenciana (FISABIO) y el Instituto Cavanilles de Biodiversidad y Biología Evolutiva de la Universitat de València València, Spain.
Front Microbiol. 2014 Jul 4;5:335. doi: 10.3389/fmicb.2014.00335. eCollection 2014.
Antibiotic therapy is a causative agent of severe disturbances in microbial communities. In healthy individuals, the gut microbiota prevents infection by harmful microorganisms through direct inhibition (releasing antimicrobial compounds), competition, or stimulation of the host's immune defenses. However, widespread antibiotic use has resulted in short- and long-term shifts in the gut microbiota structure, leading to a loss in colonization resistance in some cases. Consequently, some patients develop Clostridium difficile infection (CDI) after taking an antibiotic (AB) and, at present, this opportunistic pathogen is one of the main causes of antibiotic-associated diarrhea in hospitalized patients. Here, we analyze the composition and functional differences in the gut microbiota of C. difficile infected (CDI) vs. non-infected patients, both patient groups having been treated with AB therapy. To do so we used 16S rRNA gene and metagenomic 454-based pyrosequencing approaches. Samples were taken before, during and after AB treatment and were checked for the presence of the pathogen. We performed different analyses and comparisons between infected (CD+) vs. non-infected (CD-) samples, allowing proposing putative candidate taxa and functions that might protect against C. difficile colonization. Most of these potentially protective taxa belonged to the Firmicutes phylum, mainly to the order Clostridiales, while some candidate protective functions were related to aromatic amino acid biosynthesis and stress response mechanisms. We also found that CDI patients showed, in general, lower diversity and richness than non-infected, as well as an overrepresentation of members of the families Bacteroidaceae, Enterococcaceae, Lactobacillaceae and Clostridium clusters XI and XIVa. Regarding metabolic functions, we detected higher abundance of genes involved in the transport and binding of carbohydrates, ions, and others compounds as a response to an antibiotic environment.
抗生素治疗是微生物群落严重紊乱的一个致病因素。在健康个体中，肠道微生物群通过直接抑制（释放抗菌化合物）、竞争或刺激宿主的免疫防御来预防有害微生物的感染。然而，抗生素的广泛使用导致了肠道微生物群结构的短期和长期变化，在某些情况下导致定植抗性丧失。因此，一些患者在服用抗生素后会发生艰难梭菌感染（CDI），目前，这种机会性病原体是住院患者抗生素相关性腹泻的主要原因之一。在这里，我们分析了接受抗生素治疗的艰难梭菌感染（CDI）患者与未感染患者肠道微生物群的组成和功能差异。为此，我们使用了基于16S rRNA基因和宏基因组454焦磷酸测序的方法。在抗生素治疗前、治疗期间和治疗后采集样本，并检查病原体的存在情况。我们对感染（CD+）与未感染（CD-）样本进行了不同的分析和比较，从而提出了可能预防艰难梭菌定植的假定候选分类群和功能。这些潜在的保护性分类群大多属于厚壁菌门，主要属于梭菌目，而一些候选保护功能与芳香族氨基酸生物合成和应激反应机制有关。我们还发现，一般来说，CDI患者的多样性和丰富度低于未感染患者，而且拟杆菌科、肠球菌科、乳杆菌科以及梭菌属XI和XIVa簇的成员比例过高。关于代谢功能，我们检测到参与碳水化合物、离子和其他化合物运输和结合的基因丰度较高，这是对抗生素环境的一种反应。
